Mechanisms of cardioaccelerator action of angiotensin

Abstract

The cardioaccelerator influence of synthetic angiotensin observed in dogs having baroreceptors denervated or blood pressure buffered was studied. In dogs which had received morphine (3 mg/kg) and chloralose (90 mg/kg) and which had the sinoaortic zones denervated, angiotensin, in doses of 1 µg/kg intravenously, still caused cardiac acceleration after transection of the spinal cord at C₆ or C₇ or after removal of sym-pathetic chains bilaterally from the stellate through T₄ or T₅. In intact dogs under morphine-chloralose which had received full ganglionic blocking doses of either tetraethylammonium chloride or pentolinium tartrate, angiotensin produced marked cardiac acceleration. Administration of bretylium tosylate, in doses of 10 mg/kg intravenously, largely or completely prevented the cardioaccelerator action of angiotensin. The beta receptor blocking agents nethalide and Inderal had effects similar to those of bretylium tosylate. The studies indicate that there is a peripheral adrenergic basis for much or all of the cardiac acceleration produced by these doses of angiotensin. In the intact animal this influence would be expected to counteract much of the cardiac inhibition elicited reflexly from baroreceptors.